Absence of inducible nitric oxide synthase modulates early reperfusion-induced NF-kappaB and AP-1 activation and enhances myocardial damage. [electronic resource]
Producer: 20020319Description: 327-42 p. digitalISSN:- 1530-6860
- Animals
- Apoptosis
- Cardiotonic Agents -- metabolism
- Cytokines -- biosynthesis
- HSP70 Heat-Shock Proteins -- metabolism
- JNK Mitogen-Activated Protein Kinases
- Kinetics
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Mitogen-Activated Protein Kinases -- metabolism
- Models, Biological
- Myocardial Infarction -- enzymology
- Myocardial Reperfusion Injury -- enzymology
- Myocardium -- metabolism
- NF-kappa B -- metabolism
- Neutrophil Infiltration
- Nitric Oxide -- physiology
- Nitric Oxide Synthase -- genetics
- Nitric Oxide Synthase Type II
- Signal Transduction
- Transcription Factor AP-1 -- metabolism
- Tyrosine -- analogs & derivatives
No physical items for this record
Publication Type: Journal Article; Research Support, U.S. Gov't, P.H.S.
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